ArticleBehavioural brain research2013
Heparan sulfate deficiency in autistic postmortem brain tissue from the subventricular zone of the lateral ventricles.
Article in Behavioural brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Deciphering the microenvironment of adult neurogenesis: a perspective from neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Does Altered Membrane Glycosylation Contribute to Neurodevelopmental Dysfunction in Autism Spectrum Disorder?Membranes · 2026Review
- Heparan sulphate and neural development: dissecting the roles of astrocyte-expressed heparan sulphate.Biochemical Society transactions · 2025Review
- A synthetic HS structure selectively impairs the morphology and function of excitatory synapse by disrupting neurexin1 interactions.Glycobiology · 2025Article
- Structural pathways related to the subventricular zone are decreased in volume with altered microstructure in young adult males with autism spectrum disorder.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Glycosylation Pathways Targeted by Deregulated miRNAs in Autism Spectrum Disorder.International journal of molecular sciences · 2025Article
- Integration of structural MRI and epigenetic analyses hint at linked cellular defects of the subventricular zone and insular cortex in autism: Findings from a case study.Frontiers in neuroscience · 2022Article
- Altered expression of glycan patterns and glycan-related genes in the medial prefrontal cortex of the valproic acid rat model of autism.Frontiers in cellular neuroscience · 2022Article
- Shank3 Deficiency is Associated With Altered Profile of Neurotransmission Markers in Pups and Adult Mice.Neurochemical research · 2021Article
- Altered heparan sulfate metabolism during development triggers dopamine-dependent autistic-behaviours in models of lysosomal storage disorders.Nature communications · 2021Article
- Type IIa RPTPs and Glycans: Roles in Axon Regeneration and Synaptogenesis.International journal of molecular sciences · 2021Review
- Dysregulation of Ki-67 Expression in T Cells of Children with Autism Spectrum Disorder.Children (Basel, Switzerland) · 2021Article
- Decreased phenol sulfotransferase activities associated with hyperserotonemia in autism spectrum disorders.Translational psychiatry · 2021Article
- Glypicans and Heparan Sulfate in Synaptic Development, Neural Plasticity, and Neurological Disorders.Frontiers in neural circuits · 2021Review
- Differential Expression of Hippocampal Circular RNAs in the BTBR Mouse Model for Autism Spectrum Disorder.Molecular neurobiology · 2020Article
- Sulfate Deficiency as a Risk Factor for Autism.Journal of autism and developmental disorders · 2020Article
- Postnatal N-acetylcysteine administration rescues impaired social behaviors and neurogenesis in Slc13a4 haploinsufficient mice.EBioMedicine · 2019Article
- Epigenetic Delay in the Neurodevelopmental Trajectory of DNA Methylation States in Autism Spectrum Disorders.Frontiers in genetics · 2019Article
- The Drosophila GeneFrontiers in genetics · 2019Article
- The Biology of Regeneration Failure and Success After Spinal Cord Injury.Physiological reviews · 2018Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal cellular growth and organization have been characterized in postmortem tissue from brains of autistic individuals, suggestive of pathology in a critical neurogenic niche, the subventricular zone (SVZ) of the brain lateral ventricles (LV). We examined cellular organization, cell proliferation, and constituents of the extracellular matrix such as N-sulfated heparan sulfate (HS) and laminin (LAM) in postmortem brain tissue from the LV-SVZ of young to elderly individuals with autism (n=4) and age-matched typically developing (TD) individuals (n=4) using immunofluorescence techniques. Strong and systematic reductions in HS immunofluorescence were observed in the LV-SVZ of the TD individuals with increasing age. For young through mature, but not elderly, autistic pair members, HS was reduced compared to their matched TDs. Cellular proliferation (Ki67+) was higher in the autistic individual of the youngest age-matched pair. These preliminary data suggesting that HS may be reduced in young to mature autistic individuals are in agreement with previous findings from the BTBR T+tf/J mouse, an animal model of autism; from mice with genetic modifications reducing HS; and with genetic variants in HS-related genes in autism. They suggest that aberrant extracellular matrix glycosaminoglycan function localized to the subventricular zone of the lateral ventricles may be a biomarker for autism, and potentially involved in the etiology of the disorder.
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